CAJ | 학술논문

目的：观察穿山龙水溶性总皂苷对TNF-α加IL-17诱导的大鼠成纤维样滑膜细胞株RSC-364核转录因子NF-κB活化的调控作用及下游基因TNF-α、IL-1、ICAM-1、MMP-2、MMP-3分泌的影响。方法：用IL-17加TNF-α刺激RSC-364建立类风湿性关节炎（RA）细胞模型，以不同浓度穿山龙水溶性总皂苷干预，采用半定量RT-PCR的方法检测各组NF-κBp65基因和IκB-α基因的表达，酶联免疫吸附试验（ELISA）检测细胞培养液上清中TNF-α、IL-1、ICAM-1、MMP-2、MMP-3蛋白水平的变化。结果：穿山龙水溶性总皂苷可呈浓度依赖性抑制TNF-α加IL-17刺激的RSC-364中NF-κBp65的活化，提升IκB-α的表达，并抑制TNF-α、IL-1、ICAM-1、MMP-2、MMP-3的分泌。结论：穿山龙水溶性总皂苷可抑制NF-κB通路的活化，阻碍下游多种基因的分泌与活化，提示其可能具有抑制RA滑膜炎症的作用。
목적：관찰천산룡수용성총조감대TNF-α가IL-17유도적대서성섬유양활막세포주RSC-364핵전록인자NF-κB활화적조공작용급하유기인TNF-α、IL-1、ICAM-1、MMP-2、MMP-3분비적영향。방법：용IL-17가TNF-α자격RSC-364건립류풍습성관절염（RA）세포모형，이불동농도천산룡수용성총조감간예，채용반정량RT-PCR적방법검측각조NF-κBp65기인화IκB-α기인적표체，매련면역흡부시험（ELISA）검측세포배양액상청중TNF-α、IL-1、ICAM-1、MMP-2、MMP-3단백수평적변화。결과：천산룡수용성총조감가정농도의뢰성억제TNF-α가IL-17자격적RSC-364중NF-κBp65적활화，제승IκB-α적표체，병억제TNF-α、IL-1、ICAM-1、MMP-2、MMP-3적분비。결론：천산룡수용성총조감가억제NF-κB통로적활화，조애하유다충기인적분비여활화，제시기가능구유억제RA활막염증적작용。
This study was aimed to observe the influence of water-solubility nipponica saponin on activation of TNF-α+IL-17-induced rat fibroblast-like synovial cell line RSC-364 cellular model nuclear transcription factor NF-κB pathway as well as TNF-α, IL-1, ICAM-1, MMP-2, MMP-3 secretion. IL-17+ TNF-α were used for stimulating RSC-364 to establish rheumatoid arthritis (RA) cellular model. Water-solubility nipponica saponin in different con-centrations was used for intervention. The influence of water-solubility nipponica saponin in different concentrations on cell viability was detected by semi-quantitative RT-PCR method. Changes in the level of TNF-α, IL-1, ICAM-1, MMP-2, and MMP-3 of culture supernatant were detected by ELISA. The results showed that the activation of NF-κB p65 in RSC-364 stimulated by TNF-α+ IL-17 can be inhibited by water-solubility nipponica saponin ac-cording to its concentration. It improved IκB-α expression, and inhibited TNF-α, IL-1, ICAM-1, MMP-2 and MMP-3 secretion. It was concluded that water-solubility nipponica saponin can inhibit the activation of NF-κB pathway, hinder the secretion and activation of multiple downstream genes, which may be its effect in inhibiting syn-ovial inflammation in RA.